Zobrazeno 1 - 10
of 124
pro vyhledávání: '"Robert J. Hamm"'
Publikováno v:
Journal of Neurotrauma. 28:1185-1198
Traumatic axonal injury (TAI) is a major feature of traumatic brain injury (TBI) and is associated with much of its morbidity. To date, significant insight has been gained into the initiating pathogenesis of TAI. However, the nature of TAI within the
Autor:
Dong Sun, Zhengwen Zhou, Melissa J. McGinn, Raymond J. Colello, M. Ross Bullock, Nabil Altememi, Sarah Hagood, Robert J. Hamm, Andrew Rolfe
Publikováno v:
Journal of Neurotrauma. 27:923-938
Epidermal growth factor (EGF) is a known mitogen for neural stem and progenitor cells (NS/NPCs) in the central nervous system (CNS). In vitro, EGF maintains NS/NPCs in the proliferative state, whereas in the normal rodent brain it promotes their prol
Publikováno v:
Journal of Neurotrauma. 26:527-537
Traumatic brain injury (TBI) has been demonstrated to induce cerebral vascular dysfunction that is reflected in altered responses to various vasodilators. While previous reports have focused primarily on the short-term vascular alterations, few have
Autor:
Dong Sun, Melissa J. McGinn, Robert J. Hamm, M. Ross Bullock, Zhengwen Zhou, Raymond J. Colello, Nabil Altememi, Sarah Hagood
Publikováno v:
Experimental Neurology. 216:56-65
Stem/progenitor cells reside throughout the adult CNS and are actively dividing in the subventricular zone (SVZ) and the dentate gyrus (DG) of the hippocampus. This neurogenic capacity of the SVZ and DG is enhanced following traumatic brain injury (T
Autor:
David A. Sun, Sompong Sombati, Anya Baranova, Elisa Attkisson, Robert J. Hamm, Laxmikant S. Deshpande, Margaret S. Wilson, Robert J. DeLorenzo
Publikováno v:
Neuroscience Letters. 441:115-119
Traumatic brain injury (TBI) survivors often suffer from a post-traumatic syndrome with deficits in learning and memory. Calcium (Ca(2+)) has been implicated in the pathophysiology of TBI-induced neuronal death. However, the role of long-term changes
Autor:
Mark D. Whiting, Robert J. Hamm
Publikováno v:
Brain Research. 1213:69-77
Memory impairment is common following traumatic brain injury. However, the specific processes underlying the impairments remain unknown. Traumatic brain injury may interfere with several of the stages of the learning and memory process. In two separa
Publikováno v:
Neuroscience Letters. 436:27-30
Experimental traumatic brain injury (TBI) results in marked neurochemical and metabolic changes. Research has demonstrated that after the initial insult the brain undergoes an immediate state of hypermetabolism followed by a sustained period of hypom
Autor:
Robert J. Hamm, Margaret S. Wilson, Laxmikant S. Deshpande, David A. Sun, Anya Baranova, Sompong Sombati, Robert J. DeLorenzo
Publikováno v:
European Journal of Neuroscience. 27:1659-1672
Traumatic brain injury (TBI) survivors often suffer chronically from significant morbidity associated with cognitive deficits, behavioral difficulties and a post-traumatic syndrome and thus it is important to understand the pathophysiology of these l
Autor:
Wendy M. Reid, Robert J. Hamm
Publikováno v:
Journal of Neurotrauma. 25:248-256
Catecholaminergic neurotransmission is regionally altered following injury, and drugs aimed at these systems offer promising avenues for post-traumatic brain injury (TBI) pharmacotherapies. Atomoxetine is a selective norepinephrine transporter (NET)
Publikováno v:
Journal of Neurotrauma. 23:1233-1240
Chronic cognitive impairment is an enduring aspect of traumatic brain injury (TBI) in both humans and animals. Treating cognitive impairment in the post-traumatic stages of injury often involves the delivery of pharmacologic agents aimed at specific